Figure 7.

Model of JNK inhibition after cerebral ischemia/reperfusion. JNK activity can be elevated by activated ASK-SEK1 or MLK3-MKK-7, or be downregulated
by dephosphorylation of JNK at Thr183/Tyr185 by specific phosphatases MKP-7 following
ischemia/reperfusion. MKP-7 function is increased by its nuclear-to-cytoplasmic translocation,
which ultimately inhibits JNK activity. Active Akt (which inactivates SEK1 by phosphorylation
Ser80 and inhibits MKK-7 by MLK3 phosphorylation at Ser674) does not affect down-regulation
of JNK activity induced by MKP-7 after ischemia in the rat hippocampus.